13TH April 2016

Second most common endocrine disorder

Increased risk of miscarriage, placental abruption, hypertensive disorders, and
growth restriction.
Screening: history of thyroid disease, type 1 diabetes mellitus, or other
autoimmune disease; current or past use of thyroid therapy; or a family history of
autoimmune thyroid disease.
 First trimester:
TSH decreases in early pregnancy because of weak stimulation of TSH receptors caused
by hCG during first 12 weeeks.
T4 will then supressesTSH at hypothalamic axis.
TSH return to baselines, and then increases in third trimester
Placental growth and production of placental deiodinase

Maternal T4 transferred to the

fetus throughout the entire
pregnancy and is important for
normal fetal brain development.
(before the fetal thyroid gland
begins concentrating iodine and
synthe- sizing thyroid hormone at
approximately 12 weeks of
gestation).
 Occurs in 2% of pregnancy; Graves disease accounts of 95% of the cases.
Sx: nervousness, tremors, tachycardia, frequent stools, excessive sweating, heat
intolerance, weight loss, goiter, insomnia, palpitations, and hypertension.
Symptoms similar to normal symptoms of pregnancy or some non-thyroid-
associated diseases, hence the results of serum thyroid function tests differentiate
thyroid disease from these other possibilities.
Maternal thyrotoxicosis is associated with a greater risk of severe preeclampsia
and maternal heart failure.
 High risks of : Prem deliveries, low birth weight, and fetal loss.
Risk of development of immune-mediated hypothyroidism and hyperthyroidism in
the neonate. (antibody crosses placenta may stimulate or inhibit fetal thyroid)
Neonates of women with Graves disease treated surgically or with radioactive
iodine are at high risk of neonatal Graves disease because they lack suppresive
thioamide. (Less incidence in patient on thioamide treatment)
Routine evaluation of fetal thyroid function, including fetal thyroid ultrasonographic
assessment, umbilical cord blood sampling, or both, is not recommended
 1.7% of pregnant woman
Abnormally low TSH with normal T4
Not associated with adverse outcomes
Treatment is not recommended (antithyroid medications crosses placenta)
 Overt hypothyroidism: 0.2-1% of pregnancy
Increased TSH with decreased T4
Sx: fatigue, constipation, cold intolerance, muscle cramps, and weight gain.
Clinically: edema, dry skin, hair loss, and a prolonged relaxation phase of deep
tendon reflexes, +/- Goiter
Hashimoto thyroiditis is the most common cause of hypothyroidism in pregnancy
and is characterized by glandular destruction by autoantibodies, particularly
antithyroid peroxidase antibodies.
Adverse perinatal outcomes: spontaneous abortion, preeclampsia, preterm birth,
abruptio placen-Tae, and fetal death are associated with untreated overt
hypothyroidism
 Overt, untreated maternal hypothyroidism has been associated with an increased
risk of low birth weight and impaired neuropsychologic development of the off-
spring.
However, it is rare for maternal thyroid inhibitory antibodies to cross the placenta
and cause fetal hypothyroidism.
The prevalence of fetal hypothyroidism in the offspring of women with Hashimoto
thyroiditis is estimated to be only 1 in 180,000 neonates.
 Elevated serum TSH level in the presence of a normal free T4 level
2-5 %
unlikely to progress to overt hypothyroidism during pregnancy in otherwise
healthy women.
Currently, there is no evidence that identification and treatment of subclinical
hypothyroidism during pregnancy improves these outcomes (30).
 Universal screening not recommended.
Performed in: personal hx of thyroid disease or sx of thyroid disease, autoimmune
disease, previous delivery of infant with thyroid disease, type 1 DM, high dose neck
radiation
Not warranted for asymptomatic pregnant women who have a mildly enlarged thyroid
(because up to a 30% enlargement of the thyroid gland is typical during pregnancy)
Study demonstrated that screening and treatment of women with subclinical
hypothyroidism during pregnancy did not improve the cognitive function of their children
at age 3 years.
ACOG, Endocrine Society only recommends testing during pregnancy for those at risk of
overt hypothyroidism.
 TSH and T4
Levels of TSH
First Trimester: 0.12.5 mIU/L
Second Trimester: 0.2-3.0 mIU/L
Third Trimester: 0.3-3.0 mIU/L
Overt hyperthyroidism: low TSH, high T4
Overt hypothyroidism: high TSH, low T4
T3 toxicosis (suspect in overt hyperthyroidism with low TSH and normal FT4)
No evidence of support routine test of antithyroid antibiodies as it rarely lead to
changes in mx of women who are euthyroid / with thyroid disease. (antiTPO/antiTG
ab)
 Thionamide : Propylthiouracil (PTU) or Methimazole
Goal: lowest possible thionamides to maintain FT4 above or in high normal range,
regardless TSH. Measure FT4 2-4 weekly.
PTU: 50-150mg TDS
Prefered
Inhibits conversion of T4 to T3 and crosses the placenta less readily than methimazole
Hepatotoxicity (routine measurement not warranted)
Methimazole: 10-40mg BD/tds
a/w rare embryopathy characterized by esophageal or choanal atresia as well as aplasia cutis, a congenital
skin defect
Less risk of hepatotoxicity

Recommendation: PTU during first trimester, switch to Methimazole beginning of second

trimester
Transient leukopenia in 10% (does not require cessation)
Agranulocytosis (not related to dosage, acute onset)
Discontinue if fever or sorethroat
 FT4 replacement: Levothyroxine 1-2mcg/kg daily or 100mcg OD
Post thyroidectomy/radioiodine therapy may require higher dosage
Measured by TSH levels: 4 to 6 weeks interval
Adjust Levothyroxine by 25 to 50 mcg increment until TSH normal
Pregnancy: increase demands of T4 requirement, likely d/t oestrogen production)
Anticipatory 25% increases in T4 replacement is required.
Preconception counselling
Women with hypothyrodism should undergo TSH testing.
 Gestational transient hyperthyroidism
Women with hyperemesis gravidarum may have high T4 and low TSH
Thyroid function abnormalities result from TSH receptor stimulation from high
concentrations of hCG.
rarely symptomatic, treatment with thionamide is not recommended
May be a/w multiple gestation or molar pregnancy
Advised for expectant management
Routine measurements of thyroid function are not recommended in patients with
hyperemesis gravidarum unless other signs of overt hyperthyroidism are evident.
 Acute and life-threatening ocndition
Hyperembolic state caused by excess thyroid hormone: fever, tachycardia, cardiac
dysrhythmia, and central nervous system dysfunction.
Thyroid storm affects bodys thermoregulatory, cardiovascular, nervous, and
gastrointestinal systems, which leads to multiorgan decompensation
Heart failure and pulmonary hypertension from cardiomyopathy
Decompensation ppt by preeclampsia, anemia, or sepsis
If suspected, therapy should not be withheld pending the results.
Treatment should be carried out in intensive care areawithin a labor and delivery unit
Underlying cause should be treated.
Avoid delivery in presence of thyroid storm even if fetal status is not reassuring
 Complete Hx and Physical examination, serum TSH, USG Neck
USG neck reliably detects nodules 0.5cm
USG features: Hypoechoic pattern, irregular margins, microcalcifications
FNAC, histologic tumor markers, imunostaining
Radioiodine scanning is NOT RECOMMENDED (risk of fetal irradiation)
However, if there is administration of radioiodine before 12 weeks, fetal thyroid
gland does not become significantly functionally active until 12 weeks of gestation
and it does not appear to be at risk of damage.
Thyroidectomy (for malignancies) maybe performed before third trimester
Surgery maybe deferred to immediate postpartum period in women without
aggressive cancer dx in 3rd trimester
 Defined as thyroid dysfunction within 12 mths of delivery
Evidence of hyperthyroidism (fatigue, irritability, weight loss, palpitations, or heat intolerance),
hypothyroidism (symptoms of fatigue, constipation, or depression) or both
Transient autoimmnue thyroiditis : 5 10% of women during first year after childbirth.
New onset of abnormal levels of TSH and FT4 with 2 phases
1ST PHASE: Destruction-induced thyrotoxicosis
sx caused by excessive thyroid hormone from glandular disruption
Abrupt, small painless goiter
Thyrotoxic phase last a few months.
Treatment of thionamides: ineffective, but may consider beta blockers
2nd phase: overt hypothyroidism 4-8mth post partum
Thyromegaly, hypothyrodism
T4 replacement with Levothyroxine 25-75mcg/d for 6-12 mths
Most resolves spontaneously; 1/3 will develop permenant overt hypothyroidism.
 Thyroid Disease in Pregnancy. Practice Bulletin Number 148, Vol 125, No. 4, April
2015. The American College of Obstetricians and Gynaecology.

LEO A. CARNEY, JEFF D. QUINLAN , JANET M. WEST, MD, Thyroid Disease in

Pregnancy. Am Fam Physician. 2014 Feb 15;89(4):273-278.